Chemoceptors play a major homeostatic role during hemorrhage, shock, hypoxia, and acidosis yet the mechanism which causes the chemoceptors to discharge remains unknown. Local hypoxia, pH, pCO2, and K ion have all been implicated. Measurements of the PO2 in the carotid body of the cat with our micro O2 electrode suggest that hypoxia in the classical sense is not responsible for the discharge, but the possibility has not been eliminated. We will make additional measurements at carotid body PO2 (and pH) in vivo and in vitro under conditions of near-maximal discharge of the chemoceptors in a further attempt to test the hypoxia theory. The use of a double-barrelled microelectrode will permit simultaneous measurement of electrical potentials, injection of drugs, and/or marking of the electrode tip location. Since the hypoxia theory would seem to demand an inhomogeneous distribution of blood flow we will use the injection of silastic polymers to explore this possibility. The influence of pH, sympathetic nerve stimulation, chemicals and hormones on chemoceptor discharge and tissue PO2 will also be tested. Chemical analyses will be carried out in order to relate metabolic changes to chemoceptor discharge. Histological studies coupled with multi-parameter recordings from visualized, isolated chemoceptor units should pin-point the sensors and hopefully the mechanism of their discharge. These studies are expected to yield valuable information not only on chemoceptor discharge but also on carotid body metabolism which appears to have some unique features.